Ward – Trauma of CNS – NS Exam 2
Cranial injury:
- Sharp object (laceration) vs blunt object (fracture)
- Consequences of basal fracture (hard to see hairline fractures in base of skull on film)
o Rhinorrhea – CSF coming out your nose (can be just a tiny bit – looks like runny nose)
o Otorrhea – CSF coming out your ear(s)
o Meningitis – net result of first 2 – bugs get in (via conduit from outside to inside)
- Damage to brain:
o Frontal lobe (often clinically silent)
o Brainstem (fatal)
o Cord (disabling)
Case history – 11 yo boy hit by car – lived 6 hrs
- Brain in transverse sinus
- Brain in lung (via jugular) ( Brain emboli!! )
o Acute pulmonary infarct was seen.
Skull fractures:
- Closed, Open-bloody hole, Linear, Comminuted-bone is in
bits/fragments around fracture site, Depressed, Occult – can’t find anything sometimes even by CT or
xray.
- Kinetic energy is dissipated at suture lines (fracture doesn’t want to go through suture line – this slows the
fracture)
- Diastatic = if KE is not dissipated, fx becomes diastatic – crosses suture line = bad news
- Repeat fractures: new fracture lines do not become diastatic – healing process makes the suture line a lot
stronger than it ever was.
o Happens in alcoholics – falling all the time.
- Displaced = more than thickness of the bone (normal skull = ¼ “, can be
up to ¾ “)
- Occipital = patient is often awake
- Frontal = syncope frequent (fainting)
- Basal = blows to occiput or sides of head. Most difficult to detect
radiologically
Parenchymal Injuries: Concussion / Direct Parenchymal / Diffuse Axonal
Concussion (commonly misunderstood)
- Sudden arrest of head by rigid surface (like another fb player’s helmet) more than 3 = bad
- Transient neurologic dysfunction
o Loss of consciousness
o Cessation of breathing (temporarily)
o Loss of reflexes (not permanently)
- Pathology
o Biochemical (influx of fluid and ions, Na & K going in and out). Ionic flux.
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o Increased vascular permeability (injured a few tight junctions)
Residua: amnesia for the event or neuropsychiatric symptoms
Do not get a contusion (bruise)
Parenchymal Injury – Contusions
- Surface bruising of brain.
- Bruise: wedge-shaped, base facing point of impact
- Transmission of kinetic energy culminates in apex of triangle
One cause of subarachnoid hemorrhage
- Blood: in gray matter (gyri), in white matter, in subarachnoid space  – other cause is Berry aneurysm
- In 24 hrs – local axons swollen, neurons red (ischemia). Cytotoxic edema.
- After 24 hrs – PMNs (neutrophils), then 2nd 24 hrs macrophages (as with any
injury)
- In days – plaque jaune (yellow plaque – over site of the bruise – yellow from
hemosiderin (breakdown product)), gliosis/astrocytosis – universal response of
brain, cavitation (liquefaction necrosis d/t ischemia - macrophages leave a hole
where they ate myelin/fat/iron)
- Under frontal and temporal lobes – floors of anterior and middle fossae are
rough – sliding, shear bumps on surface of brain.
- Coup = cerebral injury at the point of contact
- Contracoup = damage to brain surface opposite to point of contact
- Parenchymal injury may also result in avulsion – (horizontal
force can cut off medulla from pons – instant death)
Coup/contracoup: IMP to know!
1. Fixed – head is fixed against wall, hit with hammer – not going
to do much damage – skull fractures, but brain is intact bc
entire calvarium was fixed
2. Movable – free standing, hit with hammer – brain wants to
stay where it is, but skull moves – inertia causes coup injury
3. Moving – as falling – brain lags behind – get contracoup
Car Injuries
- Whiplash – no cord/brain injury – sprain of anterior neck vertebral ligaments – pain goes away with
settlement
- Dashboard – glass, frame above – frontal and basal brain only - bounce back could give contracoup.
Similar to getting hit by 2x4
Rotational Injuries
- Blow to the jaw (hook from boxer) – brain slams into the sides of falx cerebri due to rotation – sort of like
a bruise in a deep gyri along falx
- Fibers that go from frontal to occipital & frontal to temporal can break
Diffuse Axonal Injury (DAI)
- Deep centroaxial white matter regions get damaged – axonal swelling & focal hemorrhagic lesions
(microscopic findings)
- Angular acceleration alone, without impact, can cause this as well as hemorrhage (swing ride at carnival)
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Lateral >>sagittal,
o Car accidents – acceleration/deceleration
o Boxing – hooks & uppercuts - sagittal
Gross Lesions: hemorrhages (petechiae) in
o Deep centroaxial white matter (Supratentorial) – corpus callosum,
paraventricular, periaqueductal, hippocampus
o Brainstem, peduncles, colliculi, deep reticular formation (in the center)
o Most obvious around central axis
o Bigger hemorrhages on the outside, petechiae toward the inside
Usually not assoc with: skull fractures, contusions, hematomas, subarachnoid
hemorrhages, low falls (short duration of acceleration)
Clinical prerequisite: coma from moment of insult (no evidence of stuff that is not assoc with DAI)
o No lucid moment
Over 50% with DAI go into coma and die in 2 weeks
Histology:
o Hemorrhages (streak, ball) – tiny petechiae
o Axonal swellings (normally like long thin hair)
o Retraction balls – axons are tightly stretched elastic bands – let go, into
little ball  swelling
o Later: gliosis, glial nodules (Babes), tract degeneration (if axons retracted,
then problem w/ this)
o glial nodule – microglia (connected w/ viral encephalitis) = Babes
o Injury at nodes of Ranvier – unprotected part of the axons, likely place to
break – cause complete cessation
of the flow of axoplasm up and
down
Traumatic Vascular Injury
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Carotid, Epidural, Subdural, Subarachnoid, Intraparenchymal, Cavernous sinus
(leading to AV fistula)
Sever carotid = immediate death
Epidural Hematoma (arterial)
o Tear of arteries in dura (middle meningeal)
 May not be assoc with fx in kids (bones are deformable) –w/o
fracture
 Hemorrhage causes dura to detach (adults) –w/ fracture
 Causes smooth compression of brain surface
(can cause SOL or  ICP)
o Lucid moment may last for several hours (wake up
from coma and seem fine, but go back into coma)
o Expansion may be rapid: emergency drainage
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Subdural Hematoma (venous)
o Target zone: space btw arachnoid and dura
o Bridging veins torn even with mild injury (more vulnerable in elderly
d/t some degree of cerebral atrophy – increases space between brain
and sinus)
 From cortex, veins course through subarachnoid, through
subdural spaces to sinuses
 a tear at junction of vein and sinus = characteristic of subdural.
(can be slow, or fast)
o Hematoma manifests clinically within 48 hrs of injury
o Mostly lateral hemispheres (10% bilateral)
o Focal vs Nonlocalizing signs (HA, confusion)
o Slowly progressive neurologic deterioration
o Pathology
 Subarachnoid space is clear (usually)
o could be xanthochromia (d/t leeching) CSF
 Clot lysis in 1 week – fibroblasts grow into hematoma from dura (2
wks)
o dura has MMA which has many of O2 to promote growth of fibroblasts
o fibroblasts generate collagen, make enough – push out fibroblasts that made it
 Hyalinized fibrous connective tissue in 1-3 months
 Forms “pita” pocket: - attached to dura, not to arachnoid
 Rebleeding common in first few months – bc when fibroblasts are growing in, new blood
vessels are growing in too, leaky neovascularization
- Intraparenchymal Hemorrhage
o Commonly assoc with: lacerations, surface contusions, high
speed car accidents (‘basal ganglion’ contusion)
o Spat Apoplexie (deep in brain) ‘late stroke’
 Rare, deep hemorrhage; may follow minor trauma (don’t
know why)
 Usually occurs after an interval of 1-2 wks
 May cause sudden death
- Subarachnoid hemorrhage
o When injury is directed at vulnerable targets: Berry aneurysms
(can get popped during an injury), vascular malformations
Sequellae of Brain Trauma
- Hydrocephalus due to – organizing SAH. (Communicating)
- Repetitive injuries, notably dementia pugilistica (punch-drunk syndrome)
o Hydrocephalus
o Thinning of corpus callosum
o Diffuse axonal injury
o Alzheimer disease (AB plaques)?
- Epilepsy – surface injury
- Psychiatric disorders
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Spinal Cord Injury
- Above C4: quadriplegia
o Respiratory paralysis
o Diaphragmatic paralysis (phrenic nerve)
- Below C4: paraplegia
o Isolated tract damage
- Hour-glass lesion
o Ascending/descending tract degeneration
- Syringomyelia (most due to Chiari type 1)
Shaken Baby Syndrome
- Subarachnoid hemorrhage
- Gliding lesion – cortex glides and shears penetrating vessels
o d/t high speed auto & shaken baby
- Intramedullary and intracordal hemorrhage
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